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Pure thalamic infarctions: Clinical findings
Pure Thalamic Infarctions: Clinical Findings Emre Kumral,
MD, PhD,
Dilek Evyapan,
MD,
and Su¨leyman Kutluhan,
MD
Our purpose in this study was to evaluate and review the risk factors, clinical profiles, and neuropsychologic abnormalities in patients with pure thalamic infarctions and to describe the clinical syndromes according to the thalamic arterial territory involved. We studied all patients with acute thalamic stroke admitted to our stroke unit over a 5-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) on all patients. We classified patients into 4 thalamic artery territory subgroups based on MRI findings: thalamogeniculate, paramedian, polar, and posterior choroidal. Patients with pure thalamic infarction represented 2.4% of patients with ischemic stroke in our registry. There were 59 patients (39 men and 20 women; mean age, 62⫾13 years) with thalamic infarctions that were confirmed by MRI. The main cause of thalamic infarction was small artery disease (75%). Hypertension (68%), hypercholesterolemia (29%), and diabetes mellitus (27%) were the most frequent risk factors. Hemisensory loss with or without motor and neuropsychologic deficit is highly associated with thalamogeniculate infarction, the most frequent type of thalamic stroke (51%). Paramedian infarction was the second most common type of thalamic infarction (34%) and is characterized by several neuropsychologic, oculomotor, and consciousness disturbances. Frontal-like syndrome with sensory motor findings is common in polar artery territory infarction (10%). Visual field defect is associated mainly with infarctions in the territory of the posterior choroidal artery (5%), probably caused by involvement of the lateral geniculate body. Approximately two thirds of the patients returned to their previous normal life. Cognitive deficits in patients with bilateral paramedian infarction persisted during the follow-up period, contrary to the other thalamic stroke subtypes. No patient died during follow-up. Acute thalamic stroke is a specific clinical picture that accurately predicts a small artery disease in the posterior circulation. The 4 arterial thalamic territories correspond well clinically to 4 different syndromes. Acute thalamic infarction appears to predict an overall good clinical recovery. Key Words: Stroke—Ischemic—Thalamus—Aphasia—Amnesia.
The thalamus is a strategic nucleus that has multiple roles in the sensory, behavioral, and motor functions, and in eye movements as well. The lesions of the thalamus can yield many syndromes depending on the thalamic
From the Cerebrovascular and Neuropsychology Unit, Department of Neurology, Ege University, Izmir, Turkey. Accepted February 8, 2000; received June 23, 2000. Address reprint requests to Emre Kumral, MD, Stroke and Neuropsychology Unit, Department of Neurology, Ege University, Bornova, Izmir, 35100, Turkey. Copyright © 2000 by National Stroke Association 1052-3057/00/0906-0005$3.00/0 doi:10.1053/jscd.2000.18741
vascular territory involved.1-6 These various clinical syndromes, characterized by prototypical clinical findings, and their pathogenetic mechanisms were reported in previous series. Most of the reported studies were based on computed tomography (CT) and neuropathologic findings.3,5,7-11 Many patients also had lesions outside of the thalamus, such as in the posterior limb of the internal capsule and centrum semiovale.2 Patients with infarctions in the territory of the anterior choroidal artery had lateral thalamic involvement with extension of the lesion to the amygdala, medial temporal lobe, and globus pallidus. In recent years, isolated thalamic infarction has generated considerable interest concerning its associated
Journal of Stroke and Cerebrovascular Diseases, Vol. 9, No. 6 (November-December), 2000: pp 287-297
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clinical characteristics, etiologic mechanisms, and nuclei involvement. We present a consecutive series of patients with pure thalamic infarctions verified by magnetic resonance imaging (MRI) and attempt to clarify the correlation between stroke etiologies, clinical features, behavioral findings, and thalamic arterial territories.
Materials and Methods We studied all patients admitted to the Ege University Hospital Stroke Unit over a 5-year period with the diagnosis of an isolated thalamic infarction. Patients with thalamic ischemic stroke represent 2.4 % of our registry, which includes 2,450 ischemic stroke patients.12 Seventyfive patients (3%) with multiple infarctions in the posterior cerebral artery (PCA) territory that involved the thalamus were excluded from analysis. MRI (with or without gadolinium contrast) and magnetic resonance angiography (MRA) were performed in all patients with thalamic ischemic stroke, and readings were performed by a neuroradiologist blinded to the findings on the neurologic and neuropsychologic evaluations. We considered only isolated thalamic infarctions with a circumscribed lesion in the thalamic nucleus. The topography of the involved thalamic nuclei groups was determined in 4 subgroups. Each subgroup was assessed by MRI by following previously published, highly detailed diagrams.13-15 The 4 groups are, as follows: 1) the anterior nuclei group, which includes the nucleus anterior principalis (Apr), nucleus fascicularis (Fa), mamillothalamic
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tract (MTT), nucleus lateropolaris (Lpo), and the nucleus paramedianus anterior (Pma); 2) the lateral nuclei group, which includes the ventral posterior lateral (or nuclei ventro-oralis intermedius [Vim], ventro-oralis externus [Voe], ventro-caudalis externus [Vce]), and ventral posterior medial nuclei (or nucleus ventro-caudalis internus [Vci]), the lateral part of the centromedian nucleus (or nucleus centralis parvo or magnocellularis), and the rostrolateral portion of the pulvinar (Pu); 3) the median nuclei group, which includes the internal medullary lamina (IML), dorsomedial nucleus (M), and the rostral interstitial nucleus of the medial longitudinal fasciculus; and 4) the posterior nuclei group, which includes the pulvinar nucleus and geniculate bodies (Fig 1). Four major vascular territories that supply the thalamic nucleus were considered, according to the templates of Percheron, Castaigne et al., and Bogousslavsky et al.1,3,7-9 They are, as follows: 1) the polar artery territory, which usually arises from the posterior communicating artery and supplies the anteromedial and anterolateral regions of the thalamus; 2) the paramedian (thalamo-subthalamic) artery territory, which arises from the proximal P1 peduncular segment of the PCA, and in about one third of brains, arises from one side or from a common pedicle and supplies the posteromedial thalamus; 3) the thalamogeniculate artery, which arises as a pedicle of 6 to 10 arteries from the P2 segment of the PCA and supplies the ventrolateral thalamus; and 4) the posterior choroidal artery, which originates from the P2 segment of the PCA and divides into the medial and lateral posterior choroidal arteries. It supplies the pulvinar and posterior thala-
Figure 1. Schematic representation of 4 arterial territories: thalamogeniculate, polar, paramedian, and posterior choroidal. The thalamic subnuclei are depicted, as follows: Apr, nucleus anterior principalis; Cemc, nucleus centralis magnocellularis; Cepc, nucleus centralis parvocellularis; Co, commisural nuclei; Dc, nucleus dorsocaudalis; Fa, nucleus fascicularis; HI, nucleus habenularislateralis, HM, nucleus hebenulais medialis; IML, internal medullary lamina; Lpo, nucleus lateropolais; M, nucleus dorsomedialis; MTM, tract of Meynert; MTT, mamillothalamic tract; Pma, nucleus paramedianus anterior; Pmp, nucleus paramedianus posterior; Pt, nucleus parataenialis; Pu, pulvinar; R, reticular nuclei; Vc, nucleus ventrocaudalis; Vim, nucleus ventro-oralis intermedius; Voe, nucleus ventro-oralis externus; Voi, nucleus ventro-oralis internus.
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mus, and the geniculate bodies, and also partly supplies the anterior nucleus (Fig 1). Systematic investigations were performed with a standard protocol including complete blood cell count and urinalysis, transcranial Doppler ultrasonography, duplex sonography of the carotid and vertebral arteries, 12-lead electrocardiography (ECG), and in selected cases, transthoracic or transesophageal echocardiography and catheter angiography. We recorded risk factors for thalamic stroke, such as hypertension (blood pressure ⬎160/90 mm Hg, at least twice before stroke), diabetes mellitus (fasting blood glucose concentrations above 6.0 mmol/L, known before stroke), regular smoking, hypercholesterolemia (fasting blood cholesterol ⬎6.5 mmol/L), venous hematocrit at admission, history of migraine and heart disease (including previous myocardial infarction, left ventricular aneurysm, hypokinesia or akinesia, chronic nonvalvular atrial fibrillation [NVAF], and mitral stenosis). We considered the following as the potential causes of thalamic ischemic stroke: 1. LAD was presumed in patients with a stenosis of at least 50% of the lumen diameter in the appropriate large artery (either vertebral or basilar artery) as shown on duplex sonography or MRA. 2. Small artery disease (SAD) was presumed in patients with longstanding hypertension or diabetes mellitus and a small (⬍15 mm) infarction limited to the territory of deep perforators of the thalamus on CT or MRI, in the absence of other etiologies. 3. Potential cardiac sources of embolism (PCSE), included mainly NVAF, left ventricular dyskinetic segment, intracardiac thrombus or tumor, mitral stenosis and other less common sources. 4. Mixed etiology was presumed in the coexistence of LAD and PCSE; 5. Other etiologies and undetermined etiologies. The neuropsychologic findings were evaluated in our neuropsychology laboratory within the first week of the stroke with a series of standardized test instruments that quantitatively measured cognitive, language, spatial, and memory functions. Short-term verbal memory was assessed by using Trials I to V of the Rey Auditory Verbal Learning Test,16 and visual recognition and memory was assessed by F form of the Benton Test.17 Frontal lobe functions were assessed by Stroop test and Luria’s conflicting task. Thalamic dementia was considered to be present if the patient has memory deficit, confabulations, lack of insight, impairment of spontaneous acting, slurred speech, flattened affect, frontal dysfunction, and a mini-mental state examination (MMSE) score below 23 points (maximum score, 30 points). We considered the following as the functional outcome of the patients: independent, mildly dependent, dependent, dead. Patients having a minor neurologic deficit,
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such as dysarthria and minimal hand or leg weakness that does not prevent performing normal activities are considered independent. Patients having a motor deficit that limits their previous activities and who need some help for walking are considered mildly dependent. Dependent patients are those who have major neurologic deficits, such as being bedridden and incontinent requiring constant nursing and attention, and those who could not return to any previous activities. Statistical data on risk factors and stroke mechanism were analyzed by using both chi-square and Fisher’s exact tests. Because of the small number of cases involved, the data on clinical features according to arterial territory were analyzed by using descriptive statistics.
Results There were 59 patients with thalamic ischemic stroke, 39 men and 20 women, with a mean age of 62⫾13 years (range, 20 to 86 years). Six patients (10%) were young (20 to 44 years) adults, and 53 (90%) were older (45 to 86 years) adults. Four of the women (20%) were over 80 years old; 1 of the men was over 80 years old, and another man (3%) was less than 30 years old. Thirty patients (51%) had an infarction in the territory of the thalamogeniculate artery, 20 (34%) in the territory of the paramedian artery (12 unilateral, 8 bilateral infarctions), 6 (10%) in the territory of the polar artery, and 3 (5%) in the territory of the posterior choroidal artery. Risk Factors In 59 patients with thalamic infarctions, the risk factors were hypertension in 69% (41 patients), hypercholesterolemia in 32% (19 patients), diabetes mellitus in 27% (16 patients), atrial fibrillation in 8% (5 patients), cigarette smoking in 17% (10 patients), and migraine in 7% (4 patients). There was a history of transient ischemic attack (TIA) in 10 patients (17%). The thalamic ischemic stroke had a nonprogressive onset of symptoms (stabilized ⬍1 hour) in 54 patients (92%), whereas it was progressive (⬎2 to 24 hours) in 5 patients (8%). Presumed Cause of Infarction SAD was diagnosed in 44 patients (75%), a source of cardiac embolism (CE) in 7 patients (12%), LAD in 2 patients (3%), and vasculitis in 1 patient (2%). The cause of stroke in 5 patients (8%) was unknown. Topography of Infarctions We identified 4 principal clinicotopographic patterns of thalamic infarction in regard to the localization of the lesion site. These are thalmogeniculate, paramedian, polar, and posterior choroidal infarctions (Tables 1 and 2).
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Table 1. Risk factors and cause of stroke in patients with pure thalamic infarction
Age (yrs ⫾ SD) Range (yrs) Gender (M/F) Hypertension Diabetes mellitus Smoking Hypercholesterolemia Atrial fibrillation Mitral valve stenosis Myocardial infarction Migraine Vasculitis Cause of stroke Large artery disease Small artery disease CSE Unknown Follow-up (mos, ⫾SD)
Thalamogeniculate infarction (n ⫽ 30)
Unilateral paramedian infarction (n ⫽ 12)
Bilateral paramedian infarction (n ⫽ 8)
Polar infarction (n ⫽ 6)
Posterior choroidal infarction (n ⫽ 3)
62 ⫾ 12 35-85 21/9 24 (80) 8 (27) 6 (20) 7 (23) 1 (3) 1 (3) 1 (3) 2 (7) 2* (7)
59 ⫾ 20 20-81 7/5 6 (50) 2 (17) 1 (8) 4 (33) 2 (17) 0 0 1 (8) 0
62 ⫾ 11 42-74 5/3 6 (75) 3 (38) 1 (13) 2 (25) 1 (13) 0 1 (13) 1 (13) 0
70 ⫾ 9 60-82 4/2 4 (67) 2 (33) 1 (17) 4 (67) 1 (17) 0 0 0 0
71 ⫾ 13 62-82 2/1 1 (33) 1 (33) 1 (33) 2 (67) 0 0 0 0 0
0 25 (83) 2 (7) 2 (7) 43 ⫾ 18
0 8 (67) 2 (17) 2 (17) 53 ⫾ 19
1 (13) 5 (63) 2 (25) 0 48 ⫾ 22
0 4 (67) 1 (17) 1 (17) 43 ⫾ 18
1 (33) 2 (67) 0 0 46 ⫾ 23
NOTE. Values in parentheses are percentage of column. Abbreviations: CSE, cardiac source of embolism. * One patient had a drug addiction.
Thalamogeniculate infarctions. Thalamogeniculate infarctions were found in 30 patients (51%). These were the most common type of infarctions (Fig 2). The stroke was completed within a few minutes in all patients, except for 1 patient in whom the stroke progressed over 30 minutes. Six patients had preceding TIAs (3 times in 1 patient). Superficial hemisensory deficit was present in all patients. Light touch sensation was reduced in 29 patients, pain sensation was abnormal in 26, and position and vibration sensations were also affected in 18 patients. Fifteen patients (50%) had motor weakness on the opposite side of the lesion. Tactile sensory loss was hemisensory in type in 8 patients, but others had fragmented deficits. Nine patients had pain sensation loss on half of their bodies, whereas other patients had deficits in different parts of the body. Three patients demonstrated hemiataxic disturbances that were characterized with dysmetria and dysdiadochokinesia. Skew deviation was present in 2 patients. Language abnormality was present in 4 patients with left thalamic lesions, and another with a right-sided lesion had anosognosia and extinction phenomenon. None of the patients had acute thalamic pain at the stroke onset, but during the follow-up period typical De´jerine-Roussy syndrome developed in 5 patients. Twenty-four patients had hypertension, 8 had diabetes mellitus, 6 were cigarette smokers (one with a history of
drug abuse), and 7 had hypercholesterolemia. One patient had mitral stenosis, and another had a previous myocardial infarction with atrial fibrillation. Twenty-five patients had lacunar infarction caused by SAD, 2 had cardiac embolisms, and 1 had vasculitis. The etiology was undetermined in 2 patients. Paramedian infarctions. Paramedian infarctions were found in 20 patients (34%). This was the second most common infarction type, present in 12 patients unilaterally and 8 patients bilaterally (Figs 3, 4A and B). Three of the patients with unilateral infarction had confusion at onset, whereas confusion or somnolence was the hallmark of the bilateral lesion group. Impairment of consciousness was usually followed by behavioral disturbances in patients with bilateral infarction. There was no dysphasia in this infarction group. Anosognosia (2 patients), extinction (1 patient), short-term visual memory deficit (4 patients), and short-term verbal amnesia (2 patients) were the neuropsychologic findings in patients with unilateral paramedian infarction, whereas in the bilateral paramedian infarction group, 4 patients had thalamic dementia. Motor and sensory dysfunctions were mild or absent in patients with unilateral and bilateral group. Ocular motor findings were more frequent and striking in patients with bilateral thalamic infarction.
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Table 2. Clinical characteristics of patients with pure thalamic infarction
Mental status abnormality Confusion Somnolence MMSE score (median ⫾ SD) Muscle strength Normal Upper limb Lower limb Upper ⫹ lower limb Face ⫹ upper limb Face ⫹ upper ⫹ lower limb Ataxia Sensory deficits Light touch Pinprick Position Vibration Cheiro-oral Cheiro-pedal De´jerine-Roussy syndrome Ocular motor deficits Upward gaze palsy Skew deviation Pseudo-VI III CNP Visual field defect (quadrantanopia) Behavioral findings Dementia Frontal dysfunction Dysphasia Verbal amnesia Visual amnesia Anosognosia/extinction Visuospatial neglect
Thalamogeniculate infarction (n ⫽ 30)
Unilateral paramedian infarction (n ⫽ 12)
Bilateral paramedian infarction (n ⫽ 8)
Polar infarction (n ⫽ 6)
Posterior choroidal infarction (n ⫽ 3)
1 (3) 1 (3) 0 27 ⫾ 1.5
3 (25) 3 (25) 0 24 ⫾ 1.7
8 (100) 5 (63) 3 (38) 21 ⫾ 3
2 (33) 2 (33) 0 24 ⫾ 2
0 0 0 28 ⫾ 1
15 (50) 0 0 1 (3) 2 (7) 12 (40) 3 (10)
7 (58) 0 0 2 (17) 1 (8) 2 (17) 3 (25)
4 (50) 0 0 0 0 3 (38)* 0
3 (50) 0 0 0 1 (17) 2 (33) 0
2 (67) 0 0 1 (33) 0 0 0
29 (97) 26 (87) 18 (60) 18 (60) 3 (10) 1 (3) 5 (17)
5 (42) 5 (42) 0 0 0 0 0
3 (38) 2 (25) 1 (13) 2 (25) 0 0 0
2 (33) 2 (33) 0 0 0 0 0
2 (66) 2 (66) 0 0 0 0 0
0 2 (7) 0 0 0
3 (25) 2 (17) 1 (8) 0 0
4 (50)† 1 (13) 1 (13) 1 (13) 0
0 0 0 0 0
0 0 0 0 2 (66)
0 0 4 0 0 1 (3) 0
0 0 0 2 (17) 4 (33) 2 (17) 0
4 (50 ) 1 (13) 0 3 (38) 3 (38) 0 0
1 (17) 3 (50) 3 (50) 2 (33) 2 (33) 0 2 (33)
0 0 0 0 0 0 0
NOTE. Values in parentheses are percentage of column. Abbreviation: III CNP, third cranial nerve palsy. *Bilateral in 2 patients. †Upward-downward palsy in 3 patients.
Twelve patients had hypertension, 5 had diabetes mellitus, 2 were cigarette smokers, and 6 had hypercholesterolemia. Three patients had atrial fibrillation, and there was excessive alcohol use in 2 patients. One patient had thyrotoxicosis, and another had cardiac dyskinesia. The etiology was undetermined in 2 patients with unilateral paramedian infarction. Four patients had cardiac embolisms, and 1 had LAD. SAD was deemed the cause of stroke in the other patients. Polar infarctions. These were present in 6 patients (10%) (Fig 5). Neuropsychologic dysfunction was the main fea-
ture in this group in contrast with the mild motor and sensory deficits. Two patients had confusion at onset. Three patients had frontal lobe dysfunctions and dysphasia. Dysphasia was characterized by a reduction of spontaneous speech, normal repetition, semantic paraphasias, mild anomia, and normal comprehension. Four patients had hypertension, 1 of them had atrial fibrillation. There was hypercholesterolemia in 4 patients, 1 was a smoker with diabetes. Cardiac embolism was considered to be an etiological factor in 1 patient. Four patients had SAD. The etiology was undetermined in 1 patient.
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term verbal recall deficit was developed after involvement of the IML, Cemc/pc, M, MTT, and MTM nuclei. Thalamic dementia developed in 5 patients who had bilateral lesions in the IML, MTT, Cemc/pc, and anterior nuclei group (1 had an infarction in the territory of the polar artery and partially in the territory of the paramedian artery; 4 had bilateral infarctions in the territory of the paramedian artery; Fig 7).
Evolution
Figure 2. T2-weighted MRI scan showing left thalamogeniculate (inferolateral) infarction in the thalamus.
Posterior choroidal infarctions. These were found in only 3 patients (5%) (Fig 6). Mental state and deep sensory modalities were normal in all patients. Motor deficit was absent or mild. Tactile and pain sensation deficits involved both the upper and lower extremities in 1 patient, and the face was also affected in another. Two patients had lower field quadrantanopia. Visual fields were normal in the other patient. One patient had hypertension alone. One patient who had diabetes mellitus also had peripheral artery disease signs and hypercholesterolemia. One patient, in addition to hypercholesterolemia, was a smoker. SAD was considered to be the etiological factor in 2 patients. The other patient had LAD.
The patients with thalamic infarctions were followed-up for up to 84 months (range, 10 to 84 months; mean, 46 ⫾18 months). None of the patients died during this period. Five of the patients with nondissociated sensory deficit developed typical De´jerine-Roussy syndrome. These patients responded mildly to amitriptyline and carbamazepine treatment. Delayed (1 month after stroke) abnormal movements of dystonia-choreiform type developed in 3 patients with thalamogeniculate territory infarctions. Among 30 patients with thalamogeniculate infarctions, at follow-up, 18 were independent, and 12 were mildly dependent. Patients with posterior choroidal infarctions fully returned to their previous life. Two of 12 patients with unilateral paramedian infarctions were partially dependent on their relatives with mild disability, whereas the others returned to their previous activities. Although, 1 of the 8 patients with bilateral paramedian infarctions had no disability, the remaining patients had severe cognitive deficits and were dependent on their families.
Thalamic Nuclei in Relation to the Sensory and Neuropsychologic Findings Patients with pinprick and light touch sensation deficits had mostly involvement of the nucleus ventrocaudalis (Vc), Vim, and Cepc. Patients having decreased sensation of position and vibration had mostly involvement of the Vc and Vim nuclei (Table 3). De´jerine-Roussy syndrome developed in patients with lesion in the Vc, Vim, and Cepc nuclei. Language disturbances were corrrelated with lesions of the Vim, Voe, Vc nuclei, and less frequently, with the involvement of the anterior nuclei group (Apr, Fa). Patients with anosognosia or neglect had involvement of Apr, IML, tract of Meynert (MTM) and Vim. Short-term visual memory/ recognition deficit was correlated with the lesion of IML, MTT, M, and nuclei centralis magnocellularis and parvocellularis (Cemc/pc) with decreasing frequency. Short-
Figure 3. T2-weighted MRI scan showing unilateral right paramedian infarction.
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Figure 4.
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T2-weighted MRI scans showing bilateral paramedian infarction. (A) Axial view. (B) Coronal view.
Four of 6 patients with polar infarctions had no disability, but the others had frontal-like syndrome, such as lack of initiation with apathy and abulia, 2 years after stroke onset.
Discussion The study of pure thalamic infarctions is useful for understanding the functions and clinical profiles of the
Figure 5. T2-weighted MRI scan showing unilateral left polar (tuberothalamic) infarction.
thalamic nucleus. We found that pure thalamic infarctions represent 2.4% of all ischemic strokes in our registry, whereas in other series, thalamic ischemic strokes constitute 3.1% to 4.4% of all ischemic strokes.3,5 Isolated thalamic stroke is not common and usually reported in older patients. Most of the reported cases with thalamic infarction had associated infarctions in other vascular territories, and concomitant multiple lesions were usually related to the presence of advanced age and a greater number of risk factors. In our series, isolated thalamic infarction occurred mostly in older adult patients, as in some studies reported previously.2,3,5,18 Ischemic thalamic stroke in young patients (⬍45 years) in our series represented 10% of all patients. In other series, thalamic infarctions in young patients account for 20% to 39% of all patients.3,5 The median age of our patients was 62 years and was similar to other series in which median ages varied from 57 to 63 years,2,3 except in 1, in which it was 48.6.5 The gender distribution in younger and older patients was similar to the finding of the Lausanne Stroke Registry, in which women predominated in the extreme age groups (⬍30 years and ⬎80 years).3 In our series, hypertension, hypercholesterolemia, diabetes mellitus, cigarette smoking, and atrial fibrillation were the most common risk factors for the ischemic thalamic lesions in order of decreasing frequency. Other rare risk factors were migraine, peripheral artery disease, alcohol abuse, and vasculitis. Several studies have shown a relationship between drug and alcohol abuse and ischemic events among young stroke patients.19-22 Migraine is a potential cause of stroke and was reported in 10% of patients with thalamic infarctions in a previous study,3
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Figure 6.
T2-weighted MRI scans showing unilateral posterior choroidal infarction.
but in our series, the frequency of migraine (7%) was lower than the others. In our study, the most frequent causes of isolated thalamic ischemic strokes were SAD in three fourths of the patients, and cardiogenic brain embolism in one tenth of patients. The frequency of large artery disease was lower in our series than in a previous study in which large artery disease was found in 7 of 40 (18%) patients with basilar or vertebral artery stenosis on angiography that might have caused artery-to-artery embolism.3 Another study reported PCA occlusion in 10% (2/20) of patients with isolated thalamic infarction.23 In our study, the frequency of infarction in the territory of the thalamogeniculate artery was higher than in the other territories of thalamic arteries, as reported previ-
ously.2,5,24,25 A possible explanation of this finding may be atherosclerotic changes frequently observed in the P2 segment of the PCA or arteriolar changes related to hypertensive arteriolopathy. The specific clinical picture of the patients with thalamogeniculate infarction was sensory and motor abnormalities with the presence of abnormal movements. We observed pure sensory deficit in one half of patients, which is similar to the previous findings.2,3,26,27 Selective loss of dorsal column sensory modalities (proprioception, stereognosis, and graphesthesia), which has been very rarely reported, was not present in our series.28 This can be explained by the fact that in the human thalamus, spinothalamic sensory (pain, temperature, and light touch) fibers localizing posteriorly
Table 3. Number and percentage of thalamic nuclei involved according to clinical symptoms
Thalamic nuclei
Pinprick (n ⫽ 37)
Light touch (n ⫽ 41)
Position (n ⫽ 19)
Vibration (n ⫽ 20)
Dysphasia (n ⫽ 6)
Anosognosia (n ⫽ 3)
Visual memory deficit (n ⫽ 9)
Apr/Pma Cemc/pc Do/Dc Fa M IML MTM MTT Pul Vim Voe Voi Vc
2 (5) 13 (35) 1 (3) 2 (5) 4 (11) 6 (16) 4 (11) 3 (8) 13 (35) 14 (38) 8 (22) 4 (11) 26 (70)
2 (5) 16 (39) 3 (7) 2 (5) 5 (12) 8 (20) 4 (10) 3 (7) 14 (34) 16 (39) 9 (22) 4 (10) 29 (71)
— 8 (42) 1 (5) — — 1 (5) 1 (5) — 9 (47) 8 (42) 3 (16) 1 (5) 17 (89)
— 8 (40) 1 (5) — — 1 (5) 1 (5) — 9 (45) 8 (40) 3 (15) 1 (5) 17 (85)
2 (33) 2 (33) — 2 (33) 1 (17) 2 (33) — 1 (17) — 4 (67) 4 (67) 1 (17) 4 (67)
— 1 (33) — — 1 (33) 2 (67) 2 (67) — 1 (33) 1 (33) — 1 (33) 1 (33)
2 (22) 4 (44) — 2 (22) 6 (67) 8 (89) 4 (44) 5 (56) — — — 3 (33) —
NOTE. No lesion is indicated by –. Values in parentheses are percentage of column. Abbreviation: Dc, n. dorsocaudalis.
Verbal memory deficit (n ⫽ 7) 2 (29) 4 (57) — 2 (29) 4 (57) 5 (71) 2 (29) 3 (43) — — — 2 (29) —
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Figure 7. Schematic location representation of sensory and cognitive deficits after thalamic infarctions. See Figure 1 for explanation of abbreviations.
in the anterior and posterior Vc subnuclei are very close to the deep sensation fibers localizing in the Vim subnucleus.14,15 We encountered the cheiro-oral-pedal or restricted acral sensory syndromes in 4 patients with lesions involving the ventralis posterior subnuclei (VP). These restricted sensory syndromes may be developed because of the involvement of the sensory projection fibers from the face, hand, and foot that are arranged from the medial to the lateral side in the ventral portion of the VP, where the tips of individual digits occupy large representation areas.29,30 One sixth of the patients with thalamogeniculate infarction affecting the ventroposterior subnuclei developed typical De´jerine-Roussy syndrome. Their response to medical treatment with carbamazepine and amitriptyline was poor. Previous studies showed that lesions of the ventroposterior nuclei (ventroposterolateral and ventroposteromedial nucleus) may cause spontaneous or evoked pain because of an imbalance of the relationships between the lateral and medial thalamic nociceptive structures and their connections with various cortical areas.31,32 The second most common type of territorial infarction was paramedian infarction, either unilaterally or bilaterally. Patients with infarction in the paramedian thalamo-
subthalamic artery territory had different degrees of altered consciousness, cognitive abnormalities, and vertical gaze paralysis, as described in previous series.1-3,5,33-37 Patients with unilateral infarctions showed only upgaze paralysis, whereas those with bilateral infarctions had both upgaze and downgaze paralysis and concomitant oculomotor dysfunctions due to involvement of the intralaminar nucleus and part of dorsomedial nucleus, with coexisting lesions of the rostral interstitial nucleus of the median longitudinal fasciculus and posterior commissure.2,3,37-40 Sensory deficits involving mostly superficial sensations were present in one third of our patients with paramedian infarctions. As reported before, the most known clinical pictures of the bilateral paramedian territory infarction are thalamic dementia, amnesia, and loss of psychic self-activation.33-35,41-45 We observed thalamic dementia in 4 patients with bilateral infarction in the thalamosubthalamic paramedian artery territory and in 1 patient with a lesion in the territory of right polar artery. Our findings are in accordance with other investigators who found that bilateral involvement of the Cemc/pc, IML, M and MMT or damage in the anterior nuclei may account for severe cognitive and memory deficits. Involvement of these structures may cause suppression of the thalamo-
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cortico-thalamic circuits centered on dorsomedialis and anterior nuclei connections with the prefrontal and cingulate lobes, and midline-intralaminar connections with neocortex and limbic brain regions.46,47 The patients with polar artery infarctions showed specific neuropsychologic deficits including apathy, disorientation, frontal dysfunction with errors on the Stroop test and Luria’s conflicting tasks, short-term verbal recall deficit and dysphasia in patients with left-sided lesions, and short-term visual recognition deficit, visuospatial neglect, and delirium in those with right-sided infarctions, as presented in previous large series.3,4,24,25 It seems that verbal memory deficit correlated well with involvement of the left nucleus dorsomedialis, IML and MMT, in the absence of significant involvement of the ventral lateral nuclei group and pulvinar. Visual memory deficit also seems to correlate with involvement of the similar nuclei on the right side. Slight and transient motor weakness predominantly in the face may be explained by the edema effect of the infarction at the initial phase of stroke. There is no strict location in the thalamus for language disturbances in our patients probably because of the multiple afferents from many thalamic regions to every area of the cortex having parallel channels of connection with the cerebral cortex and carrying different kinds of information to be used for cortico-cortical and cortico-subcortical integration of language. Analysis of patients with language difficulties in the literature showed that there is a core area centered on the anterior (Apr, Fa)- medial (M, Cemc/pc)- ventrolateral (Vim, Vc) nuclei, damage of which caused language difficulties, in most cases.48,49 Neglect and body schema disorders in patients with right thalamic lesion correspond well to the similar nuclei involved in thalamic dysphasia. The interruption of the thalamo-cortical projections coming from the anterior, medial and ventrolateral nuclei, which integrate attention to contralateral extrapersonal space and contralateral hemibody awareness, can explain the neglect and hemi-inattention. The patients with posterior choroidal artery infarctions did not have the classic visual deficits described in previous series.2,3,5,50,51 We observed inferior quadrantanopia in 2 patients, whereas the other was normal. These patients uncommonly may present with mild hemiparesis- hemihypesthesia, and in our series, 1 patient had brachiocrural hemiparesis, and 2 had superficial sensory deficit. We observed good outcome in our patients with isolated thalamic infarctions, except those with bilateral paramedian infarctions in whom cognitive deficits persisted during the follow-up. Multiple case reports as well as large series also suggested that good outcome was the rule in thalamic infarction.2,3,5 Our data concurred, 59% of our patients returned to normal without neurologic
deficit. As shown by virtually all cases in the literature,36,37,39,40,52 as well as by our own experience, the cognitive disturbances in patients with bilateral paramedian infarctions were more prominent and lasting than the unilateral lesions and other thalamic stroke subtypes. The possible explanation for this could be that the thalamus may activate both hemispheres, and cognitive disturbances caused by a thalamic lesion on one side may be compensated by the other thalamic nuclei, but damage of both thalamus may yield to persistent neuropsychologic deficits. In summary, pure thalamic stroke is a distinct clinical picture that accurately predicts a small artery disease of the posterior circulation. Pure sensory defects accurately predict a thalamogeniculate infarction. Thalamic stroke, however, can show multiple and various clinical pictures depending on the arterial territory involved. Furthermore, thalamic infarction appears to predict an overall good clinical recovery and to be a marker for cerebral small artery disease.
References 1. Castaigne P, Lhermitte F, Buge A, et al. Paramedian thalamic and midbrain infarcts: Clinical and neuropathological study. Ann Neurol 1981;10:127-148. 2. Graff-Radford NR, Damasio H, Yamada T, et al. Nonhaemorrhagic thalamic infarction: Clinical and electrophysiological findings in four anatomical groups defined by computerized tomography. Brain 1985;108: 485-516. 3. Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: Clinical syndromes, etiology, and prognosis. Neurology 1988;38:837-848. 4. Caplan LR, DeWitt LD, Pessin MS, et al. Lateral thalamic infarcts. Arch Neurol 1988;45:959-964. 5. Ocariz MMS, Nader JA, Santos JA, et al. Thalamic vascular lesions. Risk factors and clinical course for infarcts and hemorrhages. Stroke 1996;27:1530-1536. ¨ , et al. Thalamic hem6. Kumral E, Kocaer T, Ertu¨bey NO orrhage. A prospective study of 100 patients. Stroke 1995;26:964-970. 7. Percheron G. Les arta`res du thalamus humain I. Arta`res et territoire thalamiques polaires de l’arta`re communicante poste´rieure. Rev Neurol 1976; 132:297-307. 8. Percheron G. Les arta`res du thalamus humain. II. Arta`res et territoires thalamiques parame´dians de l’arta`re basilaire communicante. Rev Neurol 1976;132: 309-324. 9. Percheron G. Les arta`res du thalamus humain. Territoire des arta`res choroidienne. Rev Neurol 1977;133: 547-558. 10. Segarra JM. Cerebral vascular disease and behaviour. I. The syndrome of the mesencephalic artery (basilar artery bifurcation). Arch Neurol 1970;22:408-418. 11. Sieben G, de Reuck J, Vander Eecken H. Thrombosis of the mesencephalic artery: A clinicopathological study of 2 cases and its correlation with arterial vascularization. Acta Neurol Belg 1977;77:151-162. ¨ zkaya B, Sagduyu A, et al. The Ege Stroke 12. Kumral E, O Registry: A hospital-based study in the Aegean Region, I˙zmir, Turkey. Cerebrovasc Dis 1998;8:278-288.
PURE THALAMIC INFARCTIONS 13. Von Cramon DY, Hebel N, Schuri U. A contribution to the anatomical basis of thalamic amnesia. Brain 1985;108: 993-1008. 14. Hassler R, Riechert T. Klinische und anatomische Befunde bei streotaktischen Schmertzoperationen im Thalamus. Arch Psychiatr Nervenkr 1959;200:93-122. 15. Hirai T, Jones EG. A new parcellation of the human thalamus on the basis of histochemical staining. Brain Res Rev 1989;14:1-34. 16. Rey A. L’Examen clinique en psychologie. Paris: Press Universitaire de France, 1964. 17. Benton AL. Revised visual retention test (ed 4). San Antonio: The Psychological Corp., 1974. 18. Steinke W, Sacco RL, Mohr JP, et al. Thalamic stroke: Presentation and prognosis of infarcts and hemorrhages. Arch Neurol 1992;49:703-710. 19. Bogousslavsky J, Regi F. Ischemic stroke in adults younger than 30 years of age: Cause and prognosis. Arch Neurol 1987;44:479-482. 20. Alvarez J, Matias-Guiu J, Sumalla J, et al. Ischemic stroke in young adults: Analysis of the etiological subgroups. Acta Neurol Scand 1989;80:20-34. 21. Sloan MA, Kittner SJ, Bucholz D. Evidence of illicit drug use among young adults with first ischemic stroke. Neuroepidemiology 1991;10:98. 22. Kaku DA, Lowenstein DH. Emergence of recreational drug abuse as a major risk factor for stroke in young adults. Ann Intern Med 1990;113:821-827. 23. Goto K, Tagawa K, Uemara K, et al. Posterior cerebral artery occlusion: Clinical, CT, and angiographic correlation. Radiology 1979;132:357-368. 24. Bogousslavsky J, Regli F, Assal G. The syndrome of tuberothalamic artery territory infarction. Stroke 1986;17: 434-441. 25. Lisovski F, Koskas P, Dubard T, et al. Left tuberothalamic infarction: Neuropsychological and MRI features. Eur Neurol 1993;33:181-184. 26. Fisher CM. Thalamic pure sensory stroke. Neurology 1978;28:1141-1144. 27. Fisher CM. Pure sensory stroke and allied conditions. Stroke 1982;13:434-447. 28. Sacco RL, Bello JA, Traub R, et al. Selective proprioceptive loss from a thalamic lacunar stroke. Stroke 1987;18: 1160-1163. 29. Kim JS. Restricted acral sensory syndrome following minor stroke. Further observation with special reference to differential severity of symptoms among individual digits. Stroke 1994;25:2497-2502. 30. Kaas JH, Nelson RJ, Sur M, et al. The somatotopic organization of the ventroposterior thalamus of the squirrel monkey, Saimiri sciureus. J Comp Neurol 1984;226:111140. 31. Leijon G, Boivie J, Johansson I. Central post-stroke pain: Neurological symptoms and pain characteristics. Pain 1989;36:13-25. 32. Macchi G. Thalamic functions as interpreted from human lesions. In: Steriade M, Jones EG, McCormick DA, eds. Thalamus. Amsterdam: Elsevier, 1997:543-615. 33. Gentilini M, DeRenzi E, Crisi G. Bilateral paramdian thalamic artery infarcts: Report of eight cases. J Neurol Neurosurg Psychiatry 1987;50:900-909.
297 34. Stuss DT, Guberman A, Nelson R, et al. The neuropsychology of paramedian thalamic infarction. Brain Cogn 1988;8:348-378. 35. Bogousslavsky J, Regli F, Delaloye-Bischof A, et al. Loss of psychic self-activation with bithalamic infarction. Neurobehavioural, CT, MRI, and SPECT correlates. Acta Neurol Scand 1991;83:309-316. 36. Graff-Radford NR, Tranel D, Van Hoesen G, et al. Diencephalic amnesia. Brain 1990;113:1-25. 37. Meissner I, Sapir S, Ko¨kmen E, et al. The paramedian diencephalic syndrome: A dynamic phenomenon. Stroke 1987;18:380-385. 38. Pierrot-Deseiligny C, Chain F, Gray F, et al. Parinaud’s syndrome: Electro-oculographic and anatomical analyses of six vascular cases with deduction about vertical gaze organization in the premotor structures. Brain 1982; 105:667-696. 39. Antonini G, Rasura M, Paolini S, et al. Paramedian diencephalic syndrome. Ital J Neurol Sci 1994;15:285-290. 40. Muller JP, Deste´e A, Steinling M, et al. Infarctus bithalamique parame´dian: 1 cas avec IRM et tomographie d’e´mission gamma. Rev Neurol (Paris) 1989:145;732-734. 41. Castaigne P, Buge A, Cambier J, et al. De´mence thalamique d’origine vasculaire par ramollissement bilate´ral, limite´ au territoire de pe´dicule re´tro-mamillaire: A propos de deux observations anatomo-cliniques. Rev Neurol (Paris) 1996;114:89-107. 42. Abbruzzese G, Arata L, Bino G, et al. Thalamic dementia: Report of a case with unusual lesion location. Ital J Neurol Sci 1986;7:155-159. 43. Rondot P, de Recondo J, Davous P, et al. Infarctus thalamique bilate´ral avec mouvements anormaux et amne´sie durable. Rev Neurol (Paris) 1986;142:398-405. 44. Schott B, Mauguiere F, Laurent B, et al. L’amne´sie thalamique. Rev Neurol (Paris) 1980;136:117-130. 45. Stuss DT, Guberman A, Nelson R, et al. The neuropsychology of paramedian thalamic infarction. Brain Cogn 1988;8:348-378. 46. Rouseaux M, Steinling M, Kassiotis P, et al. De´bit sanguin ce´re´bral et infarctus thalamiques. Rev Neurol (Paris) 1989;145:140-147. 47. Baron JC, Levasseur M, Mazoyer B, et al. Thalamocortical diaschisis: Positron emission tomography in humans. J Neurol Neurosurg Psychiatry 1992;55:935-942. 48. Brown JW. Language, cognition, and the thalamus. Confin Neurol 1974;36:33-60. 49. Bruyn RPM. Thalamic aphasia. A conceptional critique. J Neurol 1989;236:21-25. 50. Besson G, Bogousslavsky J, Regli F. Posterior choroidal artery infarct with homonymous horizontal sectoranopia. Cerebrovasc Dis 1991;1:117-120. 51. Frisen L, Holmegaard L, Rosencranz M. Sectorial optic atrophy and homonymous, horizontal sectoranopia: A lateral choroidal artery syndrome? J Neurol Neurosurg Psychiatry 1978;41:364-80. 52. Baumgartner RW, Regard M. Bilateral neuropsychological deficits in unilateral paramedian thalamic infarction. Eur Neurol 1993;195-198.
MD, PhD,
Dilek Evyapan,
MD,
and Su¨leyman Kutluhan,
MD
Our purpose in this study was to evaluate and review the risk factors, clinical profiles, and neuropsychologic abnormalities in patients with pure thalamic infarctions and to describe the clinical syndromes according to the thalamic arterial territory involved. We studied all patients with acute thalamic stroke admitted to our stroke unit over a 5-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) on all patients. We classified patients into 4 thalamic artery territory subgroups based on MRI findings: thalamogeniculate, paramedian, polar, and posterior choroidal. Patients with pure thalamic infarction represented 2.4% of patients with ischemic stroke in our registry. There were 59 patients (39 men and 20 women; mean age, 62⫾13 years) with thalamic infarctions that were confirmed by MRI. The main cause of thalamic infarction was small artery disease (75%). Hypertension (68%), hypercholesterolemia (29%), and diabetes mellitus (27%) were the most frequent risk factors. Hemisensory loss with or without motor and neuropsychologic deficit is highly associated with thalamogeniculate infarction, the most frequent type of thalamic stroke (51%). Paramedian infarction was the second most common type of thalamic infarction (34%) and is characterized by several neuropsychologic, oculomotor, and consciousness disturbances. Frontal-like syndrome with sensory motor findings is common in polar artery territory infarction (10%). Visual field defect is associated mainly with infarctions in the territory of the posterior choroidal artery (5%), probably caused by involvement of the lateral geniculate body. Approximately two thirds of the patients returned to their previous normal life. Cognitive deficits in patients with bilateral paramedian infarction persisted during the follow-up period, contrary to the other thalamic stroke subtypes. No patient died during follow-up. Acute thalamic stroke is a specific clinical picture that accurately predicts a small artery disease in the posterior circulation. The 4 arterial thalamic territories correspond well clinically to 4 different syndromes. Acute thalamic infarction appears to predict an overall good clinical recovery. Key Words: Stroke—Ischemic—Thalamus—Aphasia—Amnesia.
The thalamus is a strategic nucleus that has multiple roles in the sensory, behavioral, and motor functions, and in eye movements as well. The lesions of the thalamus can yield many syndromes depending on the thalamic
From the Cerebrovascular and Neuropsychology Unit, Department of Neurology, Ege University, Izmir, Turkey. Accepted February 8, 2000; received June 23, 2000. Address reprint requests to Emre Kumral, MD, Stroke and Neuropsychology Unit, Department of Neurology, Ege University, Bornova, Izmir, 35100, Turkey. Copyright © 2000 by National Stroke Association 1052-3057/00/0906-0005$3.00/0 doi:10.1053/jscd.2000.18741
vascular territory involved.1-6 These various clinical syndromes, characterized by prototypical clinical findings, and their pathogenetic mechanisms were reported in previous series. Most of the reported studies were based on computed tomography (CT) and neuropathologic findings.3,5,7-11 Many patients also had lesions outside of the thalamus, such as in the posterior limb of the internal capsule and centrum semiovale.2 Patients with infarctions in the territory of the anterior choroidal artery had lateral thalamic involvement with extension of the lesion to the amygdala, medial temporal lobe, and globus pallidus. In recent years, isolated thalamic infarction has generated considerable interest concerning its associated
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clinical characteristics, etiologic mechanisms, and nuclei involvement. We present a consecutive series of patients with pure thalamic infarctions verified by magnetic resonance imaging (MRI) and attempt to clarify the correlation between stroke etiologies, clinical features, behavioral findings, and thalamic arterial territories.
Materials and Methods We studied all patients admitted to the Ege University Hospital Stroke Unit over a 5-year period with the diagnosis of an isolated thalamic infarction. Patients with thalamic ischemic stroke represent 2.4 % of our registry, which includes 2,450 ischemic stroke patients.12 Seventyfive patients (3%) with multiple infarctions in the posterior cerebral artery (PCA) territory that involved the thalamus were excluded from analysis. MRI (with or without gadolinium contrast) and magnetic resonance angiography (MRA) were performed in all patients with thalamic ischemic stroke, and readings were performed by a neuroradiologist blinded to the findings on the neurologic and neuropsychologic evaluations. We considered only isolated thalamic infarctions with a circumscribed lesion in the thalamic nucleus. The topography of the involved thalamic nuclei groups was determined in 4 subgroups. Each subgroup was assessed by MRI by following previously published, highly detailed diagrams.13-15 The 4 groups are, as follows: 1) the anterior nuclei group, which includes the nucleus anterior principalis (Apr), nucleus fascicularis (Fa), mamillothalamic
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tract (MTT), nucleus lateropolaris (Lpo), and the nucleus paramedianus anterior (Pma); 2) the lateral nuclei group, which includes the ventral posterior lateral (or nuclei ventro-oralis intermedius [Vim], ventro-oralis externus [Voe], ventro-caudalis externus [Vce]), and ventral posterior medial nuclei (or nucleus ventro-caudalis internus [Vci]), the lateral part of the centromedian nucleus (or nucleus centralis parvo or magnocellularis), and the rostrolateral portion of the pulvinar (Pu); 3) the median nuclei group, which includes the internal medullary lamina (IML), dorsomedial nucleus (M), and the rostral interstitial nucleus of the medial longitudinal fasciculus; and 4) the posterior nuclei group, which includes the pulvinar nucleus and geniculate bodies (Fig 1). Four major vascular territories that supply the thalamic nucleus were considered, according to the templates of Percheron, Castaigne et al., and Bogousslavsky et al.1,3,7-9 They are, as follows: 1) the polar artery territory, which usually arises from the posterior communicating artery and supplies the anteromedial and anterolateral regions of the thalamus; 2) the paramedian (thalamo-subthalamic) artery territory, which arises from the proximal P1 peduncular segment of the PCA, and in about one third of brains, arises from one side or from a common pedicle and supplies the posteromedial thalamus; 3) the thalamogeniculate artery, which arises as a pedicle of 6 to 10 arteries from the P2 segment of the PCA and supplies the ventrolateral thalamus; and 4) the posterior choroidal artery, which originates from the P2 segment of the PCA and divides into the medial and lateral posterior choroidal arteries. It supplies the pulvinar and posterior thala-
Figure 1. Schematic representation of 4 arterial territories: thalamogeniculate, polar, paramedian, and posterior choroidal. The thalamic subnuclei are depicted, as follows: Apr, nucleus anterior principalis; Cemc, nucleus centralis magnocellularis; Cepc, nucleus centralis parvocellularis; Co, commisural nuclei; Dc, nucleus dorsocaudalis; Fa, nucleus fascicularis; HI, nucleus habenularislateralis, HM, nucleus hebenulais medialis; IML, internal medullary lamina; Lpo, nucleus lateropolais; M, nucleus dorsomedialis; MTM, tract of Meynert; MTT, mamillothalamic tract; Pma, nucleus paramedianus anterior; Pmp, nucleus paramedianus posterior; Pt, nucleus parataenialis; Pu, pulvinar; R, reticular nuclei; Vc, nucleus ventrocaudalis; Vim, nucleus ventro-oralis intermedius; Voe, nucleus ventro-oralis externus; Voi, nucleus ventro-oralis internus.
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mus, and the geniculate bodies, and also partly supplies the anterior nucleus (Fig 1). Systematic investigations were performed with a standard protocol including complete blood cell count and urinalysis, transcranial Doppler ultrasonography, duplex sonography of the carotid and vertebral arteries, 12-lead electrocardiography (ECG), and in selected cases, transthoracic or transesophageal echocardiography and catheter angiography. We recorded risk factors for thalamic stroke, such as hypertension (blood pressure ⬎160/90 mm Hg, at least twice before stroke), diabetes mellitus (fasting blood glucose concentrations above 6.0 mmol/L, known before stroke), regular smoking, hypercholesterolemia (fasting blood cholesterol ⬎6.5 mmol/L), venous hematocrit at admission, history of migraine and heart disease (including previous myocardial infarction, left ventricular aneurysm, hypokinesia or akinesia, chronic nonvalvular atrial fibrillation [NVAF], and mitral stenosis). We considered the following as the potential causes of thalamic ischemic stroke: 1. LAD was presumed in patients with a stenosis of at least 50% of the lumen diameter in the appropriate large artery (either vertebral or basilar artery) as shown on duplex sonography or MRA. 2. Small artery disease (SAD) was presumed in patients with longstanding hypertension or diabetes mellitus and a small (⬍15 mm) infarction limited to the territory of deep perforators of the thalamus on CT or MRI, in the absence of other etiologies. 3. Potential cardiac sources of embolism (PCSE), included mainly NVAF, left ventricular dyskinetic segment, intracardiac thrombus or tumor, mitral stenosis and other less common sources. 4. Mixed etiology was presumed in the coexistence of LAD and PCSE; 5. Other etiologies and undetermined etiologies. The neuropsychologic findings were evaluated in our neuropsychology laboratory within the first week of the stroke with a series of standardized test instruments that quantitatively measured cognitive, language, spatial, and memory functions. Short-term verbal memory was assessed by using Trials I to V of the Rey Auditory Verbal Learning Test,16 and visual recognition and memory was assessed by F form of the Benton Test.17 Frontal lobe functions were assessed by Stroop test and Luria’s conflicting task. Thalamic dementia was considered to be present if the patient has memory deficit, confabulations, lack of insight, impairment of spontaneous acting, slurred speech, flattened affect, frontal dysfunction, and a mini-mental state examination (MMSE) score below 23 points (maximum score, 30 points). We considered the following as the functional outcome of the patients: independent, mildly dependent, dependent, dead. Patients having a minor neurologic deficit,
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such as dysarthria and minimal hand or leg weakness that does not prevent performing normal activities are considered independent. Patients having a motor deficit that limits their previous activities and who need some help for walking are considered mildly dependent. Dependent patients are those who have major neurologic deficits, such as being bedridden and incontinent requiring constant nursing and attention, and those who could not return to any previous activities. Statistical data on risk factors and stroke mechanism were analyzed by using both chi-square and Fisher’s exact tests. Because of the small number of cases involved, the data on clinical features according to arterial territory were analyzed by using descriptive statistics.
Results There were 59 patients with thalamic ischemic stroke, 39 men and 20 women, with a mean age of 62⫾13 years (range, 20 to 86 years). Six patients (10%) were young (20 to 44 years) adults, and 53 (90%) were older (45 to 86 years) adults. Four of the women (20%) were over 80 years old; 1 of the men was over 80 years old, and another man (3%) was less than 30 years old. Thirty patients (51%) had an infarction in the territory of the thalamogeniculate artery, 20 (34%) in the territory of the paramedian artery (12 unilateral, 8 bilateral infarctions), 6 (10%) in the territory of the polar artery, and 3 (5%) in the territory of the posterior choroidal artery. Risk Factors In 59 patients with thalamic infarctions, the risk factors were hypertension in 69% (41 patients), hypercholesterolemia in 32% (19 patients), diabetes mellitus in 27% (16 patients), atrial fibrillation in 8% (5 patients), cigarette smoking in 17% (10 patients), and migraine in 7% (4 patients). There was a history of transient ischemic attack (TIA) in 10 patients (17%). The thalamic ischemic stroke had a nonprogressive onset of symptoms (stabilized ⬍1 hour) in 54 patients (92%), whereas it was progressive (⬎2 to 24 hours) in 5 patients (8%). Presumed Cause of Infarction SAD was diagnosed in 44 patients (75%), a source of cardiac embolism (CE) in 7 patients (12%), LAD in 2 patients (3%), and vasculitis in 1 patient (2%). The cause of stroke in 5 patients (8%) was unknown. Topography of Infarctions We identified 4 principal clinicotopographic patterns of thalamic infarction in regard to the localization of the lesion site. These are thalmogeniculate, paramedian, polar, and posterior choroidal infarctions (Tables 1 and 2).
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Table 1. Risk factors and cause of stroke in patients with pure thalamic infarction
Age (yrs ⫾ SD) Range (yrs) Gender (M/F) Hypertension Diabetes mellitus Smoking Hypercholesterolemia Atrial fibrillation Mitral valve stenosis Myocardial infarction Migraine Vasculitis Cause of stroke Large artery disease Small artery disease CSE Unknown Follow-up (mos, ⫾SD)
Thalamogeniculate infarction (n ⫽ 30)
Unilateral paramedian infarction (n ⫽ 12)
Bilateral paramedian infarction (n ⫽ 8)
Polar infarction (n ⫽ 6)
Posterior choroidal infarction (n ⫽ 3)
62 ⫾ 12 35-85 21/9 24 (80) 8 (27) 6 (20) 7 (23) 1 (3) 1 (3) 1 (3) 2 (7) 2* (7)
59 ⫾ 20 20-81 7/5 6 (50) 2 (17) 1 (8) 4 (33) 2 (17) 0 0 1 (8) 0
62 ⫾ 11 42-74 5/3 6 (75) 3 (38) 1 (13) 2 (25) 1 (13) 0 1 (13) 1 (13) 0
70 ⫾ 9 60-82 4/2 4 (67) 2 (33) 1 (17) 4 (67) 1 (17) 0 0 0 0
71 ⫾ 13 62-82 2/1 1 (33) 1 (33) 1 (33) 2 (67) 0 0 0 0 0
0 25 (83) 2 (7) 2 (7) 43 ⫾ 18
0 8 (67) 2 (17) 2 (17) 53 ⫾ 19
1 (13) 5 (63) 2 (25) 0 48 ⫾ 22
0 4 (67) 1 (17) 1 (17) 43 ⫾ 18
1 (33) 2 (67) 0 0 46 ⫾ 23
NOTE. Values in parentheses are percentage of column. Abbreviations: CSE, cardiac source of embolism. * One patient had a drug addiction.
Thalamogeniculate infarctions. Thalamogeniculate infarctions were found in 30 patients (51%). These were the most common type of infarctions (Fig 2). The stroke was completed within a few minutes in all patients, except for 1 patient in whom the stroke progressed over 30 minutes. Six patients had preceding TIAs (3 times in 1 patient). Superficial hemisensory deficit was present in all patients. Light touch sensation was reduced in 29 patients, pain sensation was abnormal in 26, and position and vibration sensations were also affected in 18 patients. Fifteen patients (50%) had motor weakness on the opposite side of the lesion. Tactile sensory loss was hemisensory in type in 8 patients, but others had fragmented deficits. Nine patients had pain sensation loss on half of their bodies, whereas other patients had deficits in different parts of the body. Three patients demonstrated hemiataxic disturbances that were characterized with dysmetria and dysdiadochokinesia. Skew deviation was present in 2 patients. Language abnormality was present in 4 patients with left thalamic lesions, and another with a right-sided lesion had anosognosia and extinction phenomenon. None of the patients had acute thalamic pain at the stroke onset, but during the follow-up period typical De´jerine-Roussy syndrome developed in 5 patients. Twenty-four patients had hypertension, 8 had diabetes mellitus, 6 were cigarette smokers (one with a history of
drug abuse), and 7 had hypercholesterolemia. One patient had mitral stenosis, and another had a previous myocardial infarction with atrial fibrillation. Twenty-five patients had lacunar infarction caused by SAD, 2 had cardiac embolisms, and 1 had vasculitis. The etiology was undetermined in 2 patients. Paramedian infarctions. Paramedian infarctions were found in 20 patients (34%). This was the second most common infarction type, present in 12 patients unilaterally and 8 patients bilaterally (Figs 3, 4A and B). Three of the patients with unilateral infarction had confusion at onset, whereas confusion or somnolence was the hallmark of the bilateral lesion group. Impairment of consciousness was usually followed by behavioral disturbances in patients with bilateral infarction. There was no dysphasia in this infarction group. Anosognosia (2 patients), extinction (1 patient), short-term visual memory deficit (4 patients), and short-term verbal amnesia (2 patients) were the neuropsychologic findings in patients with unilateral paramedian infarction, whereas in the bilateral paramedian infarction group, 4 patients had thalamic dementia. Motor and sensory dysfunctions were mild or absent in patients with unilateral and bilateral group. Ocular motor findings were more frequent and striking in patients with bilateral thalamic infarction.
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Table 2. Clinical characteristics of patients with pure thalamic infarction
Mental status abnormality Confusion Somnolence MMSE score (median ⫾ SD) Muscle strength Normal Upper limb Lower limb Upper ⫹ lower limb Face ⫹ upper limb Face ⫹ upper ⫹ lower limb Ataxia Sensory deficits Light touch Pinprick Position Vibration Cheiro-oral Cheiro-pedal De´jerine-Roussy syndrome Ocular motor deficits Upward gaze palsy Skew deviation Pseudo-VI III CNP Visual field defect (quadrantanopia) Behavioral findings Dementia Frontal dysfunction Dysphasia Verbal amnesia Visual amnesia Anosognosia/extinction Visuospatial neglect
Thalamogeniculate infarction (n ⫽ 30)
Unilateral paramedian infarction (n ⫽ 12)
Bilateral paramedian infarction (n ⫽ 8)
Polar infarction (n ⫽ 6)
Posterior choroidal infarction (n ⫽ 3)
1 (3) 1 (3) 0 27 ⫾ 1.5
3 (25) 3 (25) 0 24 ⫾ 1.7
8 (100) 5 (63) 3 (38) 21 ⫾ 3
2 (33) 2 (33) 0 24 ⫾ 2
0 0 0 28 ⫾ 1
15 (50) 0 0 1 (3) 2 (7) 12 (40) 3 (10)
7 (58) 0 0 2 (17) 1 (8) 2 (17) 3 (25)
4 (50) 0 0 0 0 3 (38)* 0
3 (50) 0 0 0 1 (17) 2 (33) 0
2 (67) 0 0 1 (33) 0 0 0
29 (97) 26 (87) 18 (60) 18 (60) 3 (10) 1 (3) 5 (17)
5 (42) 5 (42) 0 0 0 0 0
3 (38) 2 (25) 1 (13) 2 (25) 0 0 0
2 (33) 2 (33) 0 0 0 0 0
2 (66) 2 (66) 0 0 0 0 0
0 2 (7) 0 0 0
3 (25) 2 (17) 1 (8) 0 0
4 (50)† 1 (13) 1 (13) 1 (13) 0
0 0 0 0 0
0 0 0 0 2 (66)
0 0 4 0 0 1 (3) 0
0 0 0 2 (17) 4 (33) 2 (17) 0
4 (50 ) 1 (13) 0 3 (38) 3 (38) 0 0
1 (17) 3 (50) 3 (50) 2 (33) 2 (33) 0 2 (33)
0 0 0 0 0 0 0
NOTE. Values in parentheses are percentage of column. Abbreviation: III CNP, third cranial nerve palsy. *Bilateral in 2 patients. †Upward-downward palsy in 3 patients.
Twelve patients had hypertension, 5 had diabetes mellitus, 2 were cigarette smokers, and 6 had hypercholesterolemia. Three patients had atrial fibrillation, and there was excessive alcohol use in 2 patients. One patient had thyrotoxicosis, and another had cardiac dyskinesia. The etiology was undetermined in 2 patients with unilateral paramedian infarction. Four patients had cardiac embolisms, and 1 had LAD. SAD was deemed the cause of stroke in the other patients. Polar infarctions. These were present in 6 patients (10%) (Fig 5). Neuropsychologic dysfunction was the main fea-
ture in this group in contrast with the mild motor and sensory deficits. Two patients had confusion at onset. Three patients had frontal lobe dysfunctions and dysphasia. Dysphasia was characterized by a reduction of spontaneous speech, normal repetition, semantic paraphasias, mild anomia, and normal comprehension. Four patients had hypertension, 1 of them had atrial fibrillation. There was hypercholesterolemia in 4 patients, 1 was a smoker with diabetes. Cardiac embolism was considered to be an etiological factor in 1 patient. Four patients had SAD. The etiology was undetermined in 1 patient.
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term verbal recall deficit was developed after involvement of the IML, Cemc/pc, M, MTT, and MTM nuclei. Thalamic dementia developed in 5 patients who had bilateral lesions in the IML, MTT, Cemc/pc, and anterior nuclei group (1 had an infarction in the territory of the polar artery and partially in the territory of the paramedian artery; 4 had bilateral infarctions in the territory of the paramedian artery; Fig 7).
Evolution
Figure 2. T2-weighted MRI scan showing left thalamogeniculate (inferolateral) infarction in the thalamus.
Posterior choroidal infarctions. These were found in only 3 patients (5%) (Fig 6). Mental state and deep sensory modalities were normal in all patients. Motor deficit was absent or mild. Tactile and pain sensation deficits involved both the upper and lower extremities in 1 patient, and the face was also affected in another. Two patients had lower field quadrantanopia. Visual fields were normal in the other patient. One patient had hypertension alone. One patient who had diabetes mellitus also had peripheral artery disease signs and hypercholesterolemia. One patient, in addition to hypercholesterolemia, was a smoker. SAD was considered to be the etiological factor in 2 patients. The other patient had LAD.
The patients with thalamic infarctions were followed-up for up to 84 months (range, 10 to 84 months; mean, 46 ⫾18 months). None of the patients died during this period. Five of the patients with nondissociated sensory deficit developed typical De´jerine-Roussy syndrome. These patients responded mildly to amitriptyline and carbamazepine treatment. Delayed (1 month after stroke) abnormal movements of dystonia-choreiform type developed in 3 patients with thalamogeniculate territory infarctions. Among 30 patients with thalamogeniculate infarctions, at follow-up, 18 were independent, and 12 were mildly dependent. Patients with posterior choroidal infarctions fully returned to their previous life. Two of 12 patients with unilateral paramedian infarctions were partially dependent on their relatives with mild disability, whereas the others returned to their previous activities. Although, 1 of the 8 patients with bilateral paramedian infarctions had no disability, the remaining patients had severe cognitive deficits and were dependent on their families.
Thalamic Nuclei in Relation to the Sensory and Neuropsychologic Findings Patients with pinprick and light touch sensation deficits had mostly involvement of the nucleus ventrocaudalis (Vc), Vim, and Cepc. Patients having decreased sensation of position and vibration had mostly involvement of the Vc and Vim nuclei (Table 3). De´jerine-Roussy syndrome developed in patients with lesion in the Vc, Vim, and Cepc nuclei. Language disturbances were corrrelated with lesions of the Vim, Voe, Vc nuclei, and less frequently, with the involvement of the anterior nuclei group (Apr, Fa). Patients with anosognosia or neglect had involvement of Apr, IML, tract of Meynert (MTM) and Vim. Short-term visual memory/ recognition deficit was correlated with the lesion of IML, MTT, M, and nuclei centralis magnocellularis and parvocellularis (Cemc/pc) with decreasing frequency. Short-
Figure 3. T2-weighted MRI scan showing unilateral right paramedian infarction.
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Figure 4.
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T2-weighted MRI scans showing bilateral paramedian infarction. (A) Axial view. (B) Coronal view.
Four of 6 patients with polar infarctions had no disability, but the others had frontal-like syndrome, such as lack of initiation with apathy and abulia, 2 years after stroke onset.
Discussion The study of pure thalamic infarctions is useful for understanding the functions and clinical profiles of the
Figure 5. T2-weighted MRI scan showing unilateral left polar (tuberothalamic) infarction.
thalamic nucleus. We found that pure thalamic infarctions represent 2.4% of all ischemic strokes in our registry, whereas in other series, thalamic ischemic strokes constitute 3.1% to 4.4% of all ischemic strokes.3,5 Isolated thalamic stroke is not common and usually reported in older patients. Most of the reported cases with thalamic infarction had associated infarctions in other vascular territories, and concomitant multiple lesions were usually related to the presence of advanced age and a greater number of risk factors. In our series, isolated thalamic infarction occurred mostly in older adult patients, as in some studies reported previously.2,3,5,18 Ischemic thalamic stroke in young patients (⬍45 years) in our series represented 10% of all patients. In other series, thalamic infarctions in young patients account for 20% to 39% of all patients.3,5 The median age of our patients was 62 years and was similar to other series in which median ages varied from 57 to 63 years,2,3 except in 1, in which it was 48.6.5 The gender distribution in younger and older patients was similar to the finding of the Lausanne Stroke Registry, in which women predominated in the extreme age groups (⬍30 years and ⬎80 years).3 In our series, hypertension, hypercholesterolemia, diabetes mellitus, cigarette smoking, and atrial fibrillation were the most common risk factors for the ischemic thalamic lesions in order of decreasing frequency. Other rare risk factors were migraine, peripheral artery disease, alcohol abuse, and vasculitis. Several studies have shown a relationship between drug and alcohol abuse and ischemic events among young stroke patients.19-22 Migraine is a potential cause of stroke and was reported in 10% of patients with thalamic infarctions in a previous study,3
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Figure 6.
T2-weighted MRI scans showing unilateral posterior choroidal infarction.
but in our series, the frequency of migraine (7%) was lower than the others. In our study, the most frequent causes of isolated thalamic ischemic strokes were SAD in three fourths of the patients, and cardiogenic brain embolism in one tenth of patients. The frequency of large artery disease was lower in our series than in a previous study in which large artery disease was found in 7 of 40 (18%) patients with basilar or vertebral artery stenosis on angiography that might have caused artery-to-artery embolism.3 Another study reported PCA occlusion in 10% (2/20) of patients with isolated thalamic infarction.23 In our study, the frequency of infarction in the territory of the thalamogeniculate artery was higher than in the other territories of thalamic arteries, as reported previ-
ously.2,5,24,25 A possible explanation of this finding may be atherosclerotic changes frequently observed in the P2 segment of the PCA or arteriolar changes related to hypertensive arteriolopathy. The specific clinical picture of the patients with thalamogeniculate infarction was sensory and motor abnormalities with the presence of abnormal movements. We observed pure sensory deficit in one half of patients, which is similar to the previous findings.2,3,26,27 Selective loss of dorsal column sensory modalities (proprioception, stereognosis, and graphesthesia), which has been very rarely reported, was not present in our series.28 This can be explained by the fact that in the human thalamus, spinothalamic sensory (pain, temperature, and light touch) fibers localizing posteriorly
Table 3. Number and percentage of thalamic nuclei involved according to clinical symptoms
Thalamic nuclei
Pinprick (n ⫽ 37)
Light touch (n ⫽ 41)
Position (n ⫽ 19)
Vibration (n ⫽ 20)
Dysphasia (n ⫽ 6)
Anosognosia (n ⫽ 3)
Visual memory deficit (n ⫽ 9)
Apr/Pma Cemc/pc Do/Dc Fa M IML MTM MTT Pul Vim Voe Voi Vc
2 (5) 13 (35) 1 (3) 2 (5) 4 (11) 6 (16) 4 (11) 3 (8) 13 (35) 14 (38) 8 (22) 4 (11) 26 (70)
2 (5) 16 (39) 3 (7) 2 (5) 5 (12) 8 (20) 4 (10) 3 (7) 14 (34) 16 (39) 9 (22) 4 (10) 29 (71)
— 8 (42) 1 (5) — — 1 (5) 1 (5) — 9 (47) 8 (42) 3 (16) 1 (5) 17 (89)
— 8 (40) 1 (5) — — 1 (5) 1 (5) — 9 (45) 8 (40) 3 (15) 1 (5) 17 (85)
2 (33) 2 (33) — 2 (33) 1 (17) 2 (33) — 1 (17) — 4 (67) 4 (67) 1 (17) 4 (67)
— 1 (33) — — 1 (33) 2 (67) 2 (67) — 1 (33) 1 (33) — 1 (33) 1 (33)
2 (22) 4 (44) — 2 (22) 6 (67) 8 (89) 4 (44) 5 (56) — — — 3 (33) —
NOTE. No lesion is indicated by –. Values in parentheses are percentage of column. Abbreviation: Dc, n. dorsocaudalis.
Verbal memory deficit (n ⫽ 7) 2 (29) 4 (57) — 2 (29) 4 (57) 5 (71) 2 (29) 3 (43) — — — 2 (29) —
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Figure 7. Schematic location representation of sensory and cognitive deficits after thalamic infarctions. See Figure 1 for explanation of abbreviations.
in the anterior and posterior Vc subnuclei are very close to the deep sensation fibers localizing in the Vim subnucleus.14,15 We encountered the cheiro-oral-pedal or restricted acral sensory syndromes in 4 patients with lesions involving the ventralis posterior subnuclei (VP). These restricted sensory syndromes may be developed because of the involvement of the sensory projection fibers from the face, hand, and foot that are arranged from the medial to the lateral side in the ventral portion of the VP, where the tips of individual digits occupy large representation areas.29,30 One sixth of the patients with thalamogeniculate infarction affecting the ventroposterior subnuclei developed typical De´jerine-Roussy syndrome. Their response to medical treatment with carbamazepine and amitriptyline was poor. Previous studies showed that lesions of the ventroposterior nuclei (ventroposterolateral and ventroposteromedial nucleus) may cause spontaneous or evoked pain because of an imbalance of the relationships between the lateral and medial thalamic nociceptive structures and their connections with various cortical areas.31,32 The second most common type of territorial infarction was paramedian infarction, either unilaterally or bilaterally. Patients with infarction in the paramedian thalamo-
subthalamic artery territory had different degrees of altered consciousness, cognitive abnormalities, and vertical gaze paralysis, as described in previous series.1-3,5,33-37 Patients with unilateral infarctions showed only upgaze paralysis, whereas those with bilateral infarctions had both upgaze and downgaze paralysis and concomitant oculomotor dysfunctions due to involvement of the intralaminar nucleus and part of dorsomedial nucleus, with coexisting lesions of the rostral interstitial nucleus of the median longitudinal fasciculus and posterior commissure.2,3,37-40 Sensory deficits involving mostly superficial sensations were present in one third of our patients with paramedian infarctions. As reported before, the most known clinical pictures of the bilateral paramedian territory infarction are thalamic dementia, amnesia, and loss of psychic self-activation.33-35,41-45 We observed thalamic dementia in 4 patients with bilateral infarction in the thalamosubthalamic paramedian artery territory and in 1 patient with a lesion in the territory of right polar artery. Our findings are in accordance with other investigators who found that bilateral involvement of the Cemc/pc, IML, M and MMT or damage in the anterior nuclei may account for severe cognitive and memory deficits. Involvement of these structures may cause suppression of the thalamo-
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cortico-thalamic circuits centered on dorsomedialis and anterior nuclei connections with the prefrontal and cingulate lobes, and midline-intralaminar connections with neocortex and limbic brain regions.46,47 The patients with polar artery infarctions showed specific neuropsychologic deficits including apathy, disorientation, frontal dysfunction with errors on the Stroop test and Luria’s conflicting tasks, short-term verbal recall deficit and dysphasia in patients with left-sided lesions, and short-term visual recognition deficit, visuospatial neglect, and delirium in those with right-sided infarctions, as presented in previous large series.3,4,24,25 It seems that verbal memory deficit correlated well with involvement of the left nucleus dorsomedialis, IML and MMT, in the absence of significant involvement of the ventral lateral nuclei group and pulvinar. Visual memory deficit also seems to correlate with involvement of the similar nuclei on the right side. Slight and transient motor weakness predominantly in the face may be explained by the edema effect of the infarction at the initial phase of stroke. There is no strict location in the thalamus for language disturbances in our patients probably because of the multiple afferents from many thalamic regions to every area of the cortex having parallel channels of connection with the cerebral cortex and carrying different kinds of information to be used for cortico-cortical and cortico-subcortical integration of language. Analysis of patients with language difficulties in the literature showed that there is a core area centered on the anterior (Apr, Fa)- medial (M, Cemc/pc)- ventrolateral (Vim, Vc) nuclei, damage of which caused language difficulties, in most cases.48,49 Neglect and body schema disorders in patients with right thalamic lesion correspond well to the similar nuclei involved in thalamic dysphasia. The interruption of the thalamo-cortical projections coming from the anterior, medial and ventrolateral nuclei, which integrate attention to contralateral extrapersonal space and contralateral hemibody awareness, can explain the neglect and hemi-inattention. The patients with posterior choroidal artery infarctions did not have the classic visual deficits described in previous series.2,3,5,50,51 We observed inferior quadrantanopia in 2 patients, whereas the other was normal. These patients uncommonly may present with mild hemiparesis- hemihypesthesia, and in our series, 1 patient had brachiocrural hemiparesis, and 2 had superficial sensory deficit. We observed good outcome in our patients with isolated thalamic infarctions, except those with bilateral paramedian infarctions in whom cognitive deficits persisted during the follow-up. Multiple case reports as well as large series also suggested that good outcome was the rule in thalamic infarction.2,3,5 Our data concurred, 59% of our patients returned to normal without neurologic
deficit. As shown by virtually all cases in the literature,36,37,39,40,52 as well as by our own experience, the cognitive disturbances in patients with bilateral paramedian infarctions were more prominent and lasting than the unilateral lesions and other thalamic stroke subtypes. The possible explanation for this could be that the thalamus may activate both hemispheres, and cognitive disturbances caused by a thalamic lesion on one side may be compensated by the other thalamic nuclei, but damage of both thalamus may yield to persistent neuropsychologic deficits. In summary, pure thalamic stroke is a distinct clinical picture that accurately predicts a small artery disease of the posterior circulation. Pure sensory defects accurately predict a thalamogeniculate infarction. Thalamic stroke, however, can show multiple and various clinical pictures depending on the arterial territory involved. Furthermore, thalamic infarction appears to predict an overall good clinical recovery and to be a marker for cerebral small artery disease.
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